Fisetin suppresses atherosclerosis by inhibiting ferroptosis-related oxidative stress in apolipoprotein E knockout mice.

INTRODUCTION: Fisetin has been demonstrated to inhibit the occurrence of atherosclerosis, however, the mechanism of fisetin suppressing atherosclerosis remains elusive. METHODS: The function of fisetin in the inhibition of atherosclerosis was evaluated by hematoxylin and eosin and Oil Red O staining in ApoE-/- mice. Molecular biomarkers of atherosclerosis progression were detected by Western blot and qPCR. Moreover, the inhibition of atherosclerosis on oxidative stress and ferroptosis was evaluated by immunofluorescence staining, qPCR and Western blot assays. RESULTS: The obtained results showed that serum lipid was attenuated and consequentially the formation of atherosclerosis was also suppressed by fisetin in ApoE-/- mice. Exploration of the mechanism revealed that molecular biomarkers of atherosclerosis were decreased under fisetin treatment. The level of reactive oxygen species and malondialdehyde declined, while the activity of superoxide dismutases and glutathione peroxidase was increased under the fisetin treatment. Additionally, the suppressor of ferroptosis, glutathione peroxidase 4 protein, was elevated. The ferritin was decreased in the aortic tissues treated with fisetin. CONCLUSIONS: In summary, fisetin attenuated the formation of atherosclerosis through the inhibition of oxidative stress and ferroptosis in the aortic tissues of ApoE-/- mice.

Prolyl hydroxylase inhibitor FG-4592 alleviates neuroinflammation via HIF-1/BNIP3 signaling in microglia.

BACKGROUND: Neuroinflammation is responsible for neuropsychiatric dysfunction following acute brain injury and neurodegenerative diseases. This study describes how a hypoxia-inducible factor prolyl hydroxylase (HIF-PHD) inhibitor FG-4592 prevents the lipopolysaccharide (LPS)-induced acute neuroinflammation in microglia. METHODS: The distribution of FG-4592 in mouse brain tissues was determined by collision-induced dissociation tandem mass spectrometry. Microglial activation in the hippocampus was analyzed by immunofluorescence. Moreover, we determined the activation of HIF-1 and nuclear factor-κB (NF-κB) signaling pathways, proinflammatory responses using molecular biological techniques. Transcriptome sequencing and BNIP3 silencing were conducted to explore signaling pathway and molecular mechanisms underlying FG-4592 anti-inflammatory activity. RESULTS: FG-4592 was transported into the brain tissues and LPS increased its transportation. FG-4592 promoted the expression of HIF-1α and induced the downstream gene transcription in the hippocampus. Administration with FG-4592 significantly inhibited microglial hyperactivation and decreased proinflammatory cytokine levels following LPS treatment in the hippocampus. The LPS-induced inflammatory responses and the NF-κB signaling pathway were also downregulated by FG-4592 pretreatment in microglial cells. Mechanistically, Venn diagram analysis of transcriptomic changes of BV2 cells identified that BNIP3 was a shared and common differentially expressed gene among different treatment groups. FG-4592 markedly upregulated the protein levels of BNIP3 in microglia. Importantly, BNIP3 knockdown aggravated the LPS-stimulated inflammatory responses and partially reversed the protection of FG-4592 against microglial inflammatory signaling and microglial activation in the mouse hippocampus. CONCLUSIONS: FG-4592 alleviates neuroinflammation through facilitating microglial HIF-1/BNIP3 signaling pathway in mice. Targeting HIF-PHD/HIF-1/BNIP3 axis is a promising strategy for the development of anti-neuroinflammation drugs.

Expression profile of cytokines and chemokines in a mouse high-altitude cerebral edema model.

INTRODUCTION: High-altitude cerebral edema (HACE) is considered to be the end-stage of acute mountain sickness (AMS); however, its pathophysiological mechanism remains unknown. Increasing evidences support that inflammation is an important risk factor for the occurrence of HACE. Including our published papers, previous studies demonstrated that the levels of IL-6, IL-1ß, and TNF-α in both serum and hippocampus were increased in the mouse HACE model induced by LPS stimulation combined with hypobaric hypoxia exposure; however, the expression profile of other cytokines and chemokines remains unknown. OBJECTIVE: This study was to analyze the expression profile of cytokines and chemokines in the HACE model. METHODS: The mouse HACE model was established by LPS stimulation combined with hypobaric hypoxia exposure (LH). The mice were divided into the normoxic group, LH-6 h group, LH-1 d group, and LH-7 d group. Brain water content (BWC) was determined using the wet/dry weight ratio. The levels of 30 cytokines and chemokines in the serum and hippocampal tissue were detected using LiquiChip. The mRNA expression of cytokines and chemokines in hippocampal tissue were determined by q-PCR. RESULTS: In the current study, we found that the brain water content was increased after the combinational treatment of LPS and hypobaric hypoxia. The results of LiquiChip showed that, in the serum and hippocampal tissue, most factors in all 30 cytokines and chemokines were dramatically upregulated at 6 h, and then declined at the 1st d and 7th d. Among these factors, G-CSF, M-CSF, MCP-1, KC, MIG, Eotaxin, Rantes, IP10, IL-6, MIP-2, and MIP-1ß were all increased in both serum and hippocampal tissue at 6 h. In addition, the results of q-PCR showed the mRNA levels of G-CSF, MCP-1, KC, MIG, Eotaxin, Rantes, IP10, IL-6, MIP-2, and MIP-1ß in hippocampal tissue were dramatically upregulated at 6 h. CONCLUSION: This study showed that the dynamic expression profile of 30 cytokines and chemokines in a mouse HACE model induced by LPS plus hypobaric hypoxia. The levels of G-CSF, MCP-1, KC, MIG, Eotaxin, Rantes, IP10, IL-6, MIP-2, and MIP-1ß in both serum and hippocampus were significantly increased at 6 h, which may be involved in the occurrence and development of HACE.

Correlation analysis of NT-proBNP (N-terminal probrain natriuretic peptide), 25-Hydroxyvitamin D, HMGB1(High-mobility group box 1), ACTA (endogenous activin A), blood glucose level, and electrolyte level with developmental quotient scores in neonates with hypoxic-ischemic encephalopathy.

BACKGROUND: To investigate the correlation between N-terminal probrain natriuretic peptide (NT-proBNP), 25-hydroxyvitamin D (25-(OH) D), high-mobility group box 1(HMGB1), endogenous activin A (ACTA), blood glucose level, electrolyte levels and developmental quotient (DQ) scores of Hypoxic-ischemic encephalopathy (HIE). METHODS: In this retrospective study, a total of 90 neonates diagnosed with HIE who were admitted to our hospital from January 2018 to June 2021 were retrospectively enrolled, and 40 healthy full-term neonates born in our hospital during the same period were randomly selected. Neonates with HIE and healthy conditions were set as the study group and control group, respectively. Neonates with HIE are divided into three subgroups, mild, moderate, and severe, based on the severity of HIE. The Gesell Developmental Scale (GDS) was used to assess neural development of neonates at 9 to 12 months postnatal. Biomarkers of peripheral venous blood were measured and collected in all neonates, including NT-proBNP, (25-(OH) D), HMGB1, ACTA, electrolyte levels and blood glucose levels. General demographic information and Apgar score were compared between the two groups. The differences between the two groups of biomarkers were compared and the correlation between these biomarkers and DQ scores was evaluated. RESULTS: There was no significant difference in gestational age, maternal age, gender, way of birth, birth weight, gestational age and whether the mother was a primipara between the two groups (P>0.05). The 10 min Apgar score of the study group (5.87±0.36) was lower than that of the control group (9.37±0.32) with significant difference (P<0.05). The levels of NT-proBNP, HMGB1, and ACTA in the study group were higher than that in the control group (243.87±21.29 pmol/L vs. 116.98±22.19 pmol/L; 8.92±1.87 µg/L vs. 3.28±1.08 µg/L; 23.78±0.89 ng/ml vs. 2.98±0.38 ng/ml), while the levels of 25-(OH) D and electrolyte levels were lower than that in the control group (24.28±1.87 vs. 31.29±1.93; K+: 4.49±0.23 mmol/L vs. 4.73±0.21 mmol/L; Na+: 118.76±13.02 mmol/L vs. 134.28±12.29 mmol/L; Ca2+: 1.77±0.23 mmol/L vs. 2.35±0.26 mmol/L; Mg2+: 0.61±0.17 mmol/L vs. 0.91±0.17 mmol/L), with statistically significant differences (P<0.001). The levels of NT-probNP, HMGB1, ACTA and the incidence of hypoglycemia were the highest in the severe group, which were significantly higher than those in the moderate group and mild group (P<0.05). The levels of NT-probNP, HMGB1, ACTA and the incidence of hypoglycemia were the lowest in the mild group. The 25-(OH) D level, the incidence of hyperglycemia and electrolyte levels were the lowest in the severe group, which were significantly lower than those in the moderate and mild groups (all P<0.05). Meanwhile, the 25-(OH) D level, the incidence of hyperglycemia and electrolyte levels in the moderate group were lower than those in the mild group, and the differences were statistically significant (all P<0.05). The incidence of hyperglycemia in severe group (16 cases) was the lowest, significantly lower than that in moderate group (17 cases) and mild group (22 cases), and the difference was statistically significant (all P<0.05). The DQ scores of HIE neonates were negatively correlated with NT-proBNP, HMGB1, and ACTA (r=-0.671, -0.421, -0.518, all P< 0.001). The DQ scores was positively correlated with levels of 25-(OH) D and blood glucose level (r =0.621, 0.802, all P< 0.001). The DQ scores was also positively correlated with levels of potassium, sodium, calcium and magnesium (0.367, 0.782, 0.218, 0.678, all P<0.001). CONCLUSION: The NT-proBNP, HMGB1, ACTA, 25-(OH) D, blood glucose levels and electrolyte levels are correlated with the severity of HIE, and developmental quotient scores in neonates with HIE. These biomarkers are suggestive for assessing the prognosis of neonate with HIE.

How Tourists' Perception Affects Travel Intention: Mechanism Pathways and Boundary Conditions.

Tourist subjectivities have an important effect on behavioral intentions. Under the background of normalization, tourism decision-making manifests primarily in tourists' individual preferences, which has led much research to ignore the importance of other subjective factors, as well as objective environmental factors. In the COVID-19 era, tourism behavior's social attributes have become more prominent; the effect of important others or organizations' attitudes toward tourism behavior, as well as personal knowledge, ability, and experience in preventing and controlling tourism risks, are evident. This study integrates knowledge-attitude-behavior (KAB), Theory of Perceived Risk (TPR), Social Identity Theory (SIT), and Theory of Planned Behavior (TPB), along with a comprehensive framework method, to construct an integrated model exploring the impact of knowledge, identity, and perceived risk on travel intention, to analyze its pathways and effects, to resolve the issue of mechanism, to analyze the moderating effect of past travel experience, and to answer the problem of boundary conditions. It finds that knowledge, perceived risk, and identity have a significant positive impact on travel intention; travel attitudes, subjective norms, and perceived control mediate the influence of knowledge, perceived risk, and identity on travel intention; these mechanism pathways do not always exist. The positive adjustment of past travel experiences shows that repeat visitors have a greater impact than newcomers and potential tourists.

GP-14 protects against severe hypoxia-induced neuronal injury through the AKT and ERK pathways and its induced transcriptome profiling alteration.

Gypenosides are major bioactive ingredients of G. pentaphyllum. In our previous study, we found that gypenosides had neuroprotective effects against hypoxia-induced injury. In the current study, we focused on the protective effects of gypenoside-14 (GP-14), which is one of the newly identified bioactive components, on neuronal injury caused by severe hypoxia (0.3% O2). The results showed that GP-14 pretreatment alleviated the cell viability damage and apoptosis induced by hypoxia in PC12 cells. Moreover, GP-14 pretreatment also attenuated primary neuron injuries under hypoxic conditions. Additionally, GP-14 pretreatment significantly ameliorated neuronal damage in the hippocampal region induced by high-altitude cerebral edema (HACE). At the molecular level, GP-14 pretreatment reversed the decreased activities of the AKT and ERK signaling pathways caused by hypoxia in PC12 cells and primary neurons. To comprehensively explore the possible mechanisms, transcriptome sequencing was conducted, and these results indicated that GP-14 could alter the transcriptional profiles of primary neuron. Taken together, our results suggest that GP-14 acts as a neuroprotective agent to protect against neuronal damage induced by severe hypoxia and it is a promising compound for the development of neuroprotective drugs.

NB-3 expression in endothelial cells contributes to the maintenance of blood brain barrier integrity in a mouse high-altitude cerebral edema model.

NB-3, a member of the contactin/F3 subgroup in the immunoglobulin superfamily, plays an important role in neural development and injury recovery. The blood brain barrier (BBB) is typically involved in the pathophysiology of neural disorders, such as hypoxic-ischemic brain injury. Our previous research found that NB-3 protects against brain damage in a mouse stroke model. However, its role in high-altitude disorders caused by hypobaric hypoxia exposure remains unknown. In the present study, we found that NB-3 was expressed in brain microvascular endothelial cells (BMECs) and responded to hypoxia stimulation. Conditional knockout of NB-3 in endothelial cells increased BBB leakage and downregulated tight junction proteins in vivo. NB-3 deficiency promoted the downregulation of tight junction proteins under Lipopolysaccharide (LPS)/hypoxia stimulation. Conversely, overexpression or supplementation with NB-3 alleviated endothelial barrier injuries. Transcriptome sequencing showed that NB-3 regulated various cell attachment genomic changes, including the Notch signaling pathway. Blocking the Notch signaling pathway increased VEGF/VEGFR2 pathway activation induced by LPS/hypoxia. Collectively, we present evidence that NB-3 plays key roles in maintaining BBB integrity under high-altitude cerebral edema conditions.

Multimodal Neuroimaging in Rett Syndrome With MECP2 Mutation.

Rett syndrome (RTT) is a rare neurodevelopmental disorder characterized by severe cognitive, social, and physical impairments resulting from de novo mutations in the X-chromosomal methyl-CpG binding protein gene 2 (MECP2). While there is still no cure for RTT, exploring up-to date neurofunctional diagnostic markers, discovering new potential therapeutic targets, and searching for novel drug efficacy evaluation indicators are fundamental. Multiple neuroimaging studies on brain structure and function have been carried out in RTT-linked gene mutation carriers to unravel disease-specific imaging features and explore genotype-phenotype associations. Here, we reviewed the neuroimaging literature on this disorder. MRI morphologic studies have shown global atrophy of gray matter (GM) and white matter (WM) and regional variations in brain maturation. Diffusion tensor imaging (DTI) studies have demonstrated reduced fractional anisotropy (FA) in left peripheral WM areas, left major WM tracts, and cingulum bilaterally, and WM microstructural/network topology changes have been further found to be correlated with behavioral abnormalities in RTT. Cerebral blood perfusion imaging studies using single-photon emission CT (SPECT) or PET have evidenced a decreased global cerebral blood flow (CBF), particularly in prefrontal and temporoparietal areas, while magnetic resonance spectroscopy (MRS) and PET studies have contributed to unraveling metabolic alterations in patients with RTT. The results obtained from the available reports confirm that multimodal neuroimaging can provide new insights into a complex interplay between genes, neurotransmitter pathway abnormalities, disease-related behaviors, and clinical severity. However, common limitations related to the available studies include small sample sizes and hypothesis-based and region-specific approaches. We, therefore, conclude that this field is still in its early development phase and that multimodal/multisequence studies with improved post-processing technologies as well as combined PET-MRI approaches are urgently needed to further explore RTT brain alterations.

A bioactive gypenoside (GP-14) alleviates neuroinflammation and blood brain barrier (BBB) disruption by inhibiting the NF-κB signaling pathway in a mouse high-altitude cerebral edema (HACE) model.

BACKGROUND: Neuroinflammation caused by peripheral lipopolysaccharides (LPS) under hypoxia is a key contributor to the development of high altitude cerebral edema (HACE). Our previous studies have shown that gypenosides and their bioactive compounds prevent hypoxia-induced neural injuries in vitro and in vivo. However, their effect on neuroinflammation-related HACE remains to be illustrated. The present study aimed to investigate the effects of GP-14 in HACE mouse model. METHODS: HACE mice were treated with GP-14 (100 and 200 mg/kg) for 7 days. After the treatments, the level of serum inflammation cytokines and the transcription of inflammatory factors in brain tissue were determined. The activation of microglia, astrocyte and the changes of IgG leakage and the protein levels of tight junction proteins were detected. Furthermore, the inflammatory factors and nuclear factor-κB (NF-κB) signaling pathway in BV-2 cells and primary microglia were detected. RESULTS: GP-14 pretreatment alleviated both the serum and neural inflammatory responses caused by LPS stimulation combined with hypobaric hypoxia exposure. In addition, GP-14 pretreatment inhibited microglial activation, accompanied by a decrease in the M1 phenotype and an increase in the M2 phenotype. Moreover, the disruption of the blood brain barrier (BBB) integrity, including increased IgG leakage and decreased expression of tight junction proteins, was attenuated by GP-14 pretreatment. Based on the BV-2 and primary microglial models, the inflammatory response and activation of the NF-κB signaling pathway were also inhibited by GP-14 pretreatment. CONCLUSION: Taken together, our results demonstrated that GP-14 exhibited prominent protective roles against neuroinflammation and BBB disruption in a mouse HACE model. GP-14 could be a potential choice for the treatment of HACE in the future.

The mediation of perceived risk's impact on destination image and travel intention: An empirical study of Chengdu, China during COVID-19.

Perceived risk clearly impacts travel behavior, including destination selection and satisfaction, but it is unclear how or why its effect is only significant in certain cases. This is because existing studies have undervalued the mediating factors of risk aversion, government initiatives, and media influence as well as the multiple forms or dimensions of risk that can mask its direct effect. This study constructs a structural equation model of perceived risk's impact on destination image and travel intention for a more nuanced model of the perceived risk mechanism in tourism, based on 413 e-questionnaires regarding travel to Chengdu, China during the COVID-19 pandemic, using the Bootstrap method to analyze suppressing effect. It finds that while perceived risk has a significant negative impact on destination image and travel intention, this is complexly mediated so as to appear insignificant. Furthermore, different mediating factors and dimensions of perceived risk operate differently according to their varied combinations in actual circumstances. This study is significant because it provides a theoretical interpretation of tourism risk, elucidates the mechanisms or paths by which perceived risk affects travel intention, and expands a framework for research on destination image and travel intention into the realms of psychology, political, and communication science. It additionally encourages people to pay greater attention to the negative impact of crises and focuses on the important role of internal and external responses in crisis management, which can help improve the effectiveness of crisis management and promote the sustainable development of the tourism industry.

The Clinical Efficacy of Chemotherapy Combined with Traditional Chinese Medicine in the Treatment of Cervical Cancer and Its Influence on Cellular Immunity, Serum CEA, and TNF-α.

BACKGROUND: This study aims to investigate the clinical efficacy of chemotherapy combined with traditional Chinese medicine in patients with cervical cancer and its effect on cellular immunoglobulin, serum sugar chain antigen 125 (CA125), carcinoembryonic antigen (CEA), and tumor necrosis factor-α (TNF-α). METHODS: Conventional chemotherapy was performed in control and observation groups. Meantime, the observation group received traditional Chinese medicine. Finally, the clinical efficacy, immunoglobulin, serum tumor markers, and serum TNF-α of the two groups were compared. RESULTS: Compared with the control group, total effective rate in the observation group was increased. After treatment, serum CD8+, TNF-α, CA125, and CEA levels were reduced in the two groups, and the observation group was higher. In the two groups, CD3+ and CD4+ levels were enhanced after treatment, and the observation group was also higher. Compared with the control group, the immunoglobulin IgG, IgA, and IgM levels increased in the observation group. The incidence of adverse reactions in the observation group was reduced compared to the control group. CONCLUSION: Chemotherapy combined with traditional Chinese can help improve the clinical efficacy and immunity in patients with cervical cancer. Moreover, the safety and feasibility of the treatment method are relatively high.

Inhibition of miR-337-3p involved in the protection of CoCl2 -induced injury in PC12 cells via activating JAK2/STAT3 signaling pathway.

OBJECTIVE: To investigate the possibility of microRNA (miR)-337-3p in the protection of hypoxia-induced injury in PC12 cells via modulating the JAK2/STAT3 signaling pathway. METHODS: Dual-luciferase reporter assay analyzed the relationship between the miR-337-3p and JAK2. PC12 cells were divided into normal, CoCl2 , CoCl2 + NC, CoCl2 + inhibitors, CoCl2 + JAK2, and CoCl2 + mimics + JAK2 groups. Then, PC12 cell viability and apoptosis were measured by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and Annexin-V-fluorescein isothiocyanate/propidium iodide methods. Quantitative real-time polymerase chain reaction and Western blot analysis were used to determine expressions. Besides, the intracellular reactive oxygen species (ROS) was examined by dichloro-dihydro-fluorescein diacetate (DCFH-DA) while the mitochondrial membrane potential (MMP) by using JC-1. RESULTS: The negative targeting relationship between miR-337-3p and JAK2 was confirmed. When compared with the normal group, miR-337-3p was increased while JAK2 and STAT3 were decreased in CoCl2 -induced PC12 cells, with decreased cell viability. Moreover, either miR-337-3p inhibitor or JAK2 overexpression could partially reverse CoCl2 -induced decrease in PC12 cell viability. Besides, CoCl2 could also trigger PC12 cell apoptosis by increasing cleaved caspase 3 and Bax but decreasing Bcl-2 and Bcl-XL, which, however, were abolished with the transfection of miR-337-3p inhibitors or lentivirus transfection to activate JAK2. Compared with the CoCl2 group, the average of fluorescent signals of ROS in the CoCl2 + inhibitors group and the CoCl2 + JAK2 group was lower, while the activities of superoxide dismutase, catalase, glutathione peroxidase, and total anti-oxidative capacity were higher, together with an increase in MMP. CONCLUSION: Inhibiting miR-337-3p could activate the JAK2/STAT3 signaling pathway to suppress CoCl 2 -induced cytotoxicity and apoptosis and ameliorate oxidative stress and MMP in PC12 cells.

Prognostic evaluation of child patients with infectious encephalitis through AEEG and REEG.

This study investigated prognostic evaluation of child patients with viral encephalitis through ambulatory electroencephalogram (AEEG) and regular electroencephalogram (REEG). A total of 94 child patients who were clinically diagnosed with viral encephalitis in Yantaishan Hospital of Yantai from May 2010 to July 2014, was examined with AEEG and REEG, respectively and randomly divided into AEEG group (n=47) and REEG group (n=47). The probabilities of detecting abnormal electroencephalographic activities with two examination methods were compared. The detection rates of abnormal electroencephalographic activities with AEEG and REEG were 80.0 and 65.0%, respectively, with significant differences (P<0.05); the probabilities of detecting epileptiform discharge with AEEG and REEG were 42.5 and 6.3%, respectively, with significant differences (P<0.05). The hospitalization time and time of electroencephalogram (EEG) restoring to normal of child patients with encephalitis in the REEG group were significantly longer than those of child patients with encephalitis in the AEEG group, with statistically significant differences (P<0.05). Among child patients in the AEEG group, the incidence rate of severe illness was 2.1%, and both the incidence rates of clinical recurrence and of sequela were 0. Among child patients in the REEG group, the incidence rate, clinical recurrence rate and incidence rate of sequela were 8.5, 12.7 and 8.5%, respectively, with statistically significant differences (P<0.05). To some extent, the EEG abnormality reflects the disorder degree of brain environment of child patients with viral encephalitis. The treatment effect and prognosis of child patients with viral encephalitis can be clinically evaluated based on EEG monitoring results of child patients, which has a certain clinical guiding significance. AEEG has important significance to the auxiliary diagnosis of viral encephalitis, with higher sensitivity than REEG.

Erratum: Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway.

[This corrects the article DOI: 10.3892/etm.2018.6297.].

Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway.

The present study intended to investigate the effect of fluvastatin on cardiomyocyte apoptosis after myocardial infarction in rats. Eighty myocardial infarction rat models were established and randomly divided into 4 groups (n=20): experimental group (n=20) was given fluvastatin treatment; sham operation group (n=20) and normal control group (n=20) were given saline. The dose of fluvastatin was 20 mg/(kg·d), and irrigation gavage was given for 1 week. Western blot analysis and reverse transcription-quantitative PCR (RT-qPCR) were used to detect the expression of TLR4 mRNA and protein in cardiomyocytes. TUNEL method was used to detect the apoptosis of cardiomyocytes. After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Western blot analysis showed that compared with the myocardial infarction group, the expression of TLR4 protein in normal control group, sham operation group and fluvastatin treatment group were significantly decreased, and they all were statistically significant (P<0.05). TUNEL method found that compared with the myocardial infarction group, the fluvastatin treatment group could significantly reduce the apoptosis of cardiomyocytes (19.2±3.8%), and the difference was statistically significant (P<0.05). Fluvastatin can inhibit myocardial infarction and decrease cardiomyocyte apoptosis by increasing the expression of TLR4-like receptor.

miR-211 inhibits proliferation, invasion and migration of cervical cancer via targeting SPARC.

Cervical cancer remains one of the most frequent gynecological malignancies among females around the world. Therefore, fully understanding the molecular mechanisms underlying the progression of cervical cancer may be critical for the development of effective therapeutic strategies against cervical cancer. The object was to evaluate the potential effect of miR-211 and verify its influence on the function of secreted protein acidic and rich in cysteine (SPARC) in cervical cancer. It was demonstrated that miR-211 was downregulated in cervical cancer cell lines (HeLa and C33A) and cervical cancer specimens, while SPARC expression level was higher in tumor tissues. We also revealed miR-211 upregulated expression could inhibit cells proliferation, migration and invasion in vivo. SPARC was confirmed as a direct and functional target of miR-211 and the inverse relationship between them was also observed. The results of the present study suggest that miR-211 reduced cancer growth, migration and invasion, and suppresses the SPARC expression in cervical cancer. This newly identified miR-211 may provide further insight into the progression and offers a promising target for cervical cancer therapy.

Risk Factors and Adverse Pregnancy Outcomes of Succenturiate Placenta: A Case-Control Study.

OBJECTIVE: To identify risk factors associated with succenturiate placenta and to evaluate the association between adverse pregnancy outcomes and succenturiate placenta in singleton pregnancies. STUDY DESIGN: The total population of women (n = 28,256) with singleton pregnancies who delivered in Zhangqiu City Hospital during the study period between 2002 and 2012 was reviewed. Risk factors. and adverse pregnancy outcomes were evaluated separately among women with and without succenturiate placenta by means of χ² and logistic regression analyses. RESULTS: The incidence of succenturiate placenta among women with singleton pregnancies was 1.04% (n = 294 of 28,256). Independent risk factors for succenturiate placenta were gestational age, prepregnancy BMI, pelvic infection, prior cesarean section, infertility, and preeclampsia. The succenturiate placenta was associated with a 1.076-, 1.056-, 12.076-, 1.894-, 5.217-, and 4.814-fold increased risk, respectively, as compared to pregnancies with normal cord insertion. For pregnancy outcome comparisons, cases of premature birth, low birth weight, and 5-minute Apgar score ≤ 7 were higher in cases with succenturiate placenta than in those without succenturiate placenta. The rate of cesarean section was increased. CONCLUSION: The results suggest that the incidence of succenturiate placenta increases along with an increase in pelvic infection, infertility, and preeclampsia. The condition of succenturiate placenta increases the risks for prematurity, impaired fetal growth, and cesarean delivery.

EMMNet: sensor networking for electricity meter monitoring.

Smart sensors are emerging as a promising technology for a large number of application domains. This paper presents a collection of requirements and guidelines that serve as a basis for a general smart sensor architecture to monitor electricity meters. It also presents an electricity meter monitoring network, named EMMNet, comprised of data collectors, data concentrators, hand-held devices, a centralized server, and clients. EMMNet provides long-distance communication capabilities, which make it suitable suitable for complex urban environments. In addition, the operational cost of EMMNet is low, compared with other existing remote meter monitoring systems based on GPRS. A new dynamic tree protocol based on the application requirements which can significantly improve the reliability of the network is also proposed. We are currently conducting tests on five networks and investigating network problems for further improvements. Evaluation results indicate that EMMNet enhances the efficiency and accuracy in the reading, recording, and calibration of electricity meters.

[Dexamethasone up-regulates the expression of glucocorticoid receptor in growth plate and inhibits the longitudinal growth of bone: experiment with rats].

OBJECTIVE: To investigate the regulation of the glucocorticoid of pharmacological doses on the expression of glucocorticoid receptor in growth plate and to explore the mechanism of the direct inhibition of the longitudinal growth of bone by dexamethasone. METHODS: Twenty 3-week-old male weanling SD rats were randomly divided into two groups: dexamethasone group (n = 12), intraperitoneally injected with dexamethasone 200 microg/100 g body weight once a day for 10 days and control group (n = 8), intraperitoneally injected with normal saline of the same volume. Ten days later the rats were killed. The length of the proximal tibia was excised, fixed and decalcified, and then paraffin embedded. Sections of 5 microm thick were cut and processed for histomorphometry The total height of growth plate, height of proliferative zone, and height of hypertrophic zone were determined. RESULTS: The length of tibia, total height of growth plate, height of proliferative zone, and height of hypertrophic zone of the dexamethasone group were 28.9 mm +/- 1.2 mm, 4.01 microm +/- 0.28 microm, 1.98 microm +/- 0.13 microm, and 1.67 microm +/- 0.18 microm respectively, all significantly lower those of the control group (30.5 mm +/- 1.1 mm, 5.53 microm +/- 0.46 microm, 2.25 microm +/- 0.30 microm, and 2.87 microm +/- 0.19 microm respectively, all P < 0.01). The resting chondrocytes and hypertrophic chondrocytes in the growth plates of the rats in the dexamethasone group all expressed glucocorticoid receptor, whereas the proliferating chondrocytes didn't. The absorbance values of the resting chondrocytes and hypertrophic chondrocytes in the growth plates of the dexamethasone group were 0.238 +/- 0.026 and 0.283 +/- 0.042 respectively, both significantly higher than those of the control group (0.187 +/- 0.027 and 0.211 +/- 0.022 respectively, both P < 0.01). CONCLUSION: The glucocorticoid receptors are essential for the longitudinal growth of bone. The glucocorticoid of pharmacological dose inhibits the longitudinal growth of bone by up-regulating the expression of glucocorticoid receptor.